Consecuencias sobre la salud y la función respiratoria del tratamiento químico del agua en piscinas cubiertas (Consequences to health and lung function of the chemical treatments of water in indoor swimming pools)

El objetivo de este trabajo fue identificar los tratamientos químicos del agua utilizados en piscinas cubiertas y los métodos para evaluar sus efectos en la función y aparato respiratorio de diferentes poblaciones asistentes a estas instalaciones. Se realizó una búsqueda de publicaciones científicas y libros sobre los tratamientos químicos en piscinas y sus efectos en la salud y la función respiratoria. Los tratamientos químicos en piscina basados en el cloro y el bromo generan subproductos de desinfección dañinos para el organismo (DBPs) como las cloraminas y los trihalomentanos (THM). Existen tratamientos alternativos como ultravioleta y ozono que reducen la formación de DBPs. Los métodos de evaluación utilizados para detectar enfermedades, daño pulmonar y de las vías respiratorias son las técnicas basadas en la espirometría, y el análisis de biomarcadores en plasma o suero sanguíneo (proteínas CC16, surfactantes A, B y D, Inmunoglobulina específica), aire exhalado (óxido nítrico, citoquinas), orina (CC16, leukotrieno B4), esputo o saliva (eosinofilos y linfocitos) y DBPs en aire exhalado, sangre u orina. Los efectos observados en las diferentes poblaciones han sido el aumento de la permeabilidad del epitelio pulmonar, la inflamación de las vías respiratorias y síntomas asociados al asma, hiper-reactividad bronquial y rinitis alérgica. Los efectos negativos detectados en el aparato respiratorio de las diferentes poblaciones en piscinas están relacionados con la exposición a productos químicos. Algunos Biomarcadores (como la proteína CC16) obtienen una mayor fiabilidad. Los tratamientos complementarios (ozono y ultravioleta) no han sido evaluados y pueden suponer una reducción en los problemas respiratorios de nadadores y trabajadores.Palabras Clave: biomarcadores, enfermedades respiratorias, espirometría, natación, subproductos de desinfección.Abstrac: The aim of this study was to identify the effects on respiratory function produced by water chemical treatments in the indoor pools in different populations. We made a review of the scientific literature about chemical treatments of water and assessment methods used to detect health effects and respiratory function. Chemical treatments chlorine and bromine generate disinfection byproducts (DBPs) that are harmful to the body, such as chloramines and trihalomethanes (THM). There exist alternative treatments such as ultraviolet radiation and ozone to reduce the formation of DBPs. The methods used to detect diseases of the respiratory tract are spirometry, analysis of biomarkers in plasma or serum (CC16 proteins, surfactants A, B and D, etc..) and exhaled air (nitric oxide, cytokines). The health problems that have been observed are the increase in lung epithelial permeability, inflammation of the airways and other symptoms associated with asthma, allergic rhinitis and bronchial hyper reactivity. The negative effects on respiratory function are related to prolonged exposure to chemicals (chlorine and bromine) in indoor swimming pools. Some biomarkers such as protein CC16 obtain greater reliability as a measurable variable. The reduced presence of DBPs in combination water treatments may be a way to reduce respiratory problems. However, more research is needed for confirmation.Key words: biomarkers, disinfection by products, lung diseases, spirometry, swimming.

Asbestos-induced lung epithelial permeability: potential role of nonoxidant pathways

Asbestos fibers are an important cause of lung fibrosis; however, the biological mechanisms are incompletely understood. The lung epithelium serves an important barrier function in the lung, and disrupting the epithelial barrier can contribute to lung fibrosis. Lung epithelial permeability is increased in patients with asbestosis, and asbestos fibers increase permeability across cultured human lung epithelium. However, the mechanism of this increased permeability is not known. Many of the biological effects of asbestos are postulated to be due to its ability to generate oxidants, and oxidants are known to increase epithelial permeability. However, we previously reported that altering the iron content of asbestos (important in oxidant generation) had no effect on its ability to increase permeability. For that reason, we undertook these studies to determine whether asbestos increases epithelial permeability through nonoxidant pathways. Both extracellular (H2O2) and intracellular (menadione) oxidants increase paracellular permeability across human lung epithelial monolayers. Extracellular catalase but not superoxide dismutase prevented increased permeability after both oxidant exposures. However, catalase offered no protection from asbestos-induced permeability. We next depleted the cells of glutathione or catalase to determine whether depleting normal cellular antioxidants would increase the sensitivity to asbestos. Permeability was the same in control cells and in cells depleted of these antioxidants. In addition to generating oxidants, asbestos also activates signal transduction pathways. Blocking protein kinase C activation did not prevent asbestos-induced permeability; however, blocking tyrosine kinase with tyrophostin A25 did prevent asbestos-induced permeability, and blocking tyrosine phosphatase with sodium vanadate enhanced the effect of asbestos. These data demonstrate that asbestos may increase epithelial permeability through nonoxidant pathways that involve tyrosine kinase activation. This model offers an important system for studying pathways involved in regulating lung epithelial permeability.